525 patho exam 1 (set two)
Terms
undefined, object
copy deck
- single layer of epithelial cells of the heart (outermost)
- epicardium
- layer of cardiac myocytes and connective tissue (middle layer)
- myocardium
- single layer of endothelial cells (inside layer)
- endocardium
- the sac the heart sits in; composed of connective tissue with a few ml of fluid for lubrication
- pericardial sac
- when fluid collects inside the sac and the heart cannot fill or pump
- cardiac tamponade
- these allow for the unidirectional movement of blood in the heart
- valves
- how do valves open and close?
- pressure differences
- valve that separates the left ventricle and left atria
- mitral (bicuspid)
- valve that separates right ventricle and right atria
- tricuspid
- what holds mitral and tricuspid valve leaflets in place?
- chordae tendineae attached to papillary muscles
- to allow for filling during ventricular relaxation and prevent blood from regurgitating into the atria during ventricular contraction
- Purpose of mitral and tricuspid valves
- why are the papillary muscle cells among the first to depolarize?
- to tense the valve to prevent the valve from failing during ventricular contraction
-
during heart contraction, these allow blood to move from the ventricles into the pulmonary trunk and aorta;
during relaxation they prevent blood from moving back into ventricles - semilunar valves
- During ventricular contraction when the semilunar valves open, why do their leaflets flap over the openings to the coronary arteries?
- to prevent blood from entering during ventricular contraction because the pressure is too high; coronary arteries receive their blood during ventricular relaxation when semilunar valves are in the closed position
- Striated muscle fibers associated with the heart; have actin and myosin arranged in sarcomeres; cells are shorter, branched, and have a single nucleus
-
myocardium
*a cardiac muscle fiber is made up of many individual cells (not one cell, like skeletal muscle) - individual cells joined together to form a fiber or disc with numerous gap junctions
- intercalated disc
- what is the purpose of gap junctions in the myocardium?
- electrical events in one cell are transmitted to others by means of gap junctions; AP in one cell can influence other cells and thus propagate from cell to cell throughout the heart by means of the gap junctions
- Does the heart beat at a constant rate and volume?
-
no
-Heart is highly regulated.
-Rich neural innervation
-Responds to hormones. - these nerves release norepinephrine
- sympathetic fibers
- the receptors that norepinephrine and epinephrine bind to
- beta-adrenergic receptors
- this hormone is from the adrenal medulla, binds to the same recetors, thus acting like norepinephrine
- epinephrine
- what is the net result of beta-adrenergic receptor binding of norepinephrine/epinephrine?
- increased heart rate and force of contraction
- these neurons release acetylcholine
- parasympathetic fibers
- what does acetylcholine do?
- binds to receptors that slow the heart
- these drugs bind and block beta adrenergic receptors
-
beta blockers
-slow heart rate and reduce force of contraction - Why would it be a poor design to deliver blood to the heart muscle directly from the left ventricle?
- too much pressure and coronary arteries would have to be huge
-
1.to provide a uniform and abundant blood supply to the myocardium
2.to deliver oxygen, nutrients, remove CO2 and other waste products - purpose of coronary circulation
- results in more than one artery perfusing the same tissue
- anastomoses
- the leading cause of death in the US
- coronary artery disease
- what causes coronary artery disease (cardivascular disease)?
- atherosclerosis
- begins at an early age and develops over many years and considered a chronic inflammatory disease
- atherosclerosis
-
modifiable:
high fat diet
high serum cholesterol (<160 mg/dL considered good)
high LDL
low HDL
smoking (increased fibrinogen levels in smokers, increases LDL and decreases HDL)
hypertension - especially elevated systolic - risk factors associated with CAD (CVD)
- this is white, elevated and partially blocks the lumen - occur at bifurcations, curvatures, and at narrowings
- plaque
- these are thought to develop into plaque
-
fatty streaks
*fatty streak formation can start as early as 10 -
-occurs with 75% blockage of coronary artery
-ischemia and angina pectoris - first appearance of symptoms of CAD
-
1.if severe ischemia occurs,
2.necrosis of the myocardium results (MI)
3.plaques may become hemorrhagic
4.lead to thrombosis
or
3.plaques may calcify(dystrophic-causes inflammation from an area of unresolved healing)
- pathogenesis of CAD
- If a thrombus blocks the artery it can result in
- sudden unstable angina or an MI
- If a thrombus embolizes and blocks the coronary artery at a more distal site, this is called
- acute coronary syndrome
-
1.drug Tx: nitroglycerin, beta blockers
2.CABG
3.angioplasty - treatment of CAD to restore blood flow
- dilates arteries and reduce peripheral resistance
- nitroglycerin (nitric oxide)
- this drug reduces work load on the heart
- beta blockers (slows heart and force of contraction)
- these drugs prevent thrombosis
-
Ca channel blockers
aspirin -
-a less invasive procedure
-quick recovery
-local anesthesia
insert a catheter into the femoral, brachial, or carotid artery and snake it to coronary artery openings at base of aorta, cath. w/baloon pushes plaques against vessel wall - angioplasty
-
-much more invasive
-major surgery through the sternum and opening of the pericardium and stopping the heart
-venous or arterial graft from leg
-sewn into the aorta and bypasses the blockage to the artery to restor blood supply distal to t -
CABG
coronary artery bypass graft (bypass surgery) - conditions which results when the blood supply is not able to meet metabolic demands of myocardium
- inschemic heart disease (aka mycardial ischemia)
- angina pectoris and myocardial infarction
- symptoms of ischemic heart disease
- Perception of pain in ischemic heart disease is thought to be related to what mechanism?
- Lactic acid, the waste product of the glycolytic pathway to produce ATP, builds up when oxygen is not available and stimulates nerve endings.
- Where is pain perceived from ischemic heart disease?
-
Angina or MI pain:
substernal, feeling of tightness, crushing pain, may radiate down one or both arms into neck and jaw
pallow, dyspnea, profuse sweating
in women: fatigue -
means "to choke"
refers to chest pain or pressure associated with myocardial ischemia
radiates to jaw and left arm ("referred pain" travels common neurons from these areas) - Angina
- what are the three kinds of angina?
-
classic angina
variant angina
unstable angina -
-occurs in people with CAD in which exertion above normal activity increases metabolic needs of the heart, but demand exceeds supply
-with rest or vasodilator, chest pain diminishes (myocardial demand decreases) - classic angina (exertional, stable)
-
In an otherwise healthy individual,this results from coronary artery spasm (constriction) that results in myocardial ischemia; usually at night or at rest
-may occur in people without any evidence of CAD
-may occur in people who can run a mile - variant angina (atypical)
-
-Occurs in people with a prior history of classic angina in which the pain does not subside at rest
-Occurs in people with a prior history of classic angina with activity which in the past did not result in angina
-or angina occurs even at rest -
unstable angina
*a worsening of the normal pattern of angina pain - ischemic necrosis of myocardium, n usually results from prolonged ischemia - 20-40 minutes (depends on the amount of anastomoses).
- Myocardial Infarction (MI)
- this is influence by the extent, severity, and duration of ischemmic episode and the metabolic needs of the myocardium at the time of the event
-
size of infarct
*the larger the infarct the greater the loss of contractility - why do infarcts usually occur in the left ventricle?
-
left ventricle works the hardest
*MI results in decreased ventricular function -
1.central area of necrosis
2.surrounded by an area of injury
3.which is surrounded by an area of ischemia - the sum of 1-3 determines amount or area of myocardial dysfunction from an MI
- area of necrosis from MI is replaced by what?
- scar tissue, since cardiac myocytes cannot regenerate
- what is the significance of the negative impact of scar tissue in the myocardium?
- scar inhibits tissue contractility and the significance of this depends on the amount of scar tissue formed; as contractility falls, heart failure ensues
- what are the compensatory mechanisms initiated to maintain cardiac output?
-
peripheral vascular constriction
heart rate increase
renal retention of sodium and water
activation of renin-angiotensin system -
-these range from sudden death to dysrhythmias, ventricular rupture, to no symptoms or vague symptoms such as fatigue or acute symptoms
-Acute symptoms include acute substernal pain, diaphoresis, dyspnea, nausea, vomiting, and anxiety -
Clinical Manifestations of a Myocardial Infarction (MI)
*n depends on severity of infarct, previous physical condition, previous infarcts, location of infarct -
LABS:
-CBC elevated leukocytes
-fever
-elevated erythrocyte sedimentation rate
-myoglobin in serum
-Creatine Kinase (CK-MB)
-Troponin - (CTnT) - lab levels indicative of Myocardial Infarction (MI)
- Why is cardia troponin (CTnT) the best marker of the occurence of an MI?
- it is found only in cardiac cells; it is a regulatory protein that mediates contraction in cardiac muscle
- a serum protein released by cells in response to acute injury, infection or other inflammatory stimuli
- C-reactive Protein (CRP)
- why is CRP significant?
-
people with athersclerosis make and release CRP, may serve as a predictor of CAD in addition to serum cholesterol levels, especially for people with low cholesterol.
CRP also promotes atherosclerosis formation
CRP>3mg/L is considered high risk for CVD -
diseases in which valve function and the flow of blood through the heart is compromised; accompanied by
-stenosis
-cardiac muscle hypertrophy - valvular disease
- heart valve orifice narrows and leaflets fuse; results in obstruction to blood flow
-
stenosis
*chambers try to compensate for stenosis - when heart chambers must compensate for stenosis by increasing pressure this leads to a thickening of heart muscle fibers called
- cardiac muscle hypertrophy
- this results from scarring and retraction of the valve leaflets - retrograde flow of blood (regurgitation)
- cadiac insufficiency
- when stenosis and regurgitation occur simultaneously, the defect is called a...
- mixed lesion and is considered to be an advanced disease
-
impairment of blood flow from the left atrium to the left ventricle
when valve cannot open during diastole. - mitral stenosis
-
-most common cause - scarring from rheumatic fever
-other cause - congenital stenosis, bacterial endocarditis - causes of mitral stenosis
-
-valve becomes funnel shaped
-rarely any symptoms until the valve orifice is decreased from 4-6 to 1-2 cm
-pulmonary symptoms are see first
-left atria dilates and hypertrophies - mitral stenosis
- mitral stenosis leads to
-
1.pulmonary edema
2.increased pressure on right heart-right heart hypertrophy
3.progresses to right heart failure - if pulmonary hypertension is sufficient to cause blood to exit the pulmonary circuit
- hemoptysis - blood in sputum
-
-Rare condition – occurs for the same reasons as mitral stenosis
-5% of all patients with rheumatic fever will develop tricuspid stenosis - tricuspid stenosis
-
Peripheral edema
organomegaly
ascities
jugular venous distension
dyspnea
tiredness - symptoms of right heart failure
- backflow of blood from the left ventricle across the mitral valve to the left atrium during ventricular systole because mitral valve fails to close
- Mitral regurgitation and insufficiency
-
common: mitral valve prolapse, coronary artery disease and rheumatic valve disease
less common: include connective tissue disease, papillary muscle dysfunction (why?) and infective endocarditis - causes of mitral regurgitation and insufficiency
- how is mitral regurgitation and insufficiency diagnosed?
-
-no symptoms for many years - then signs of congestive heart failure develop
-systolic murmur
-(with rupture of papillary muscle, onset is very rapid, and see sudden onset of pulmonary congestion and pulmonary edema) -
-rare condition
-backflow of blood from the right ventricle across the tricuspid valve to the right atrium during ventricular systole and tricuspid valve fails to close - Tricuspid regurgitation
- most common causes of this condition are enlargement of the right ventricle (many causes), rheumatic fever, bacterial endocarditis (IV drug abusers), diet medication called “phen-fen†(dexfenfluramine)
-
causes of triscupid regurgitation
*symptoms are the same as tricuspid stenosis - -both the conditions of narrowed mitral opening and failure of the mitral valve to close properly caused by rheumatic lesions
-
Mixed mitral stenosis and regurgitation
*symptoms are the same as those associated with either mitral stenosis or regurgitation -
-condition is probably a congenital abnormality (women, or marfan syndrome)caused by a posterior displacement of the posterior cusp of the mitral valve
-large posterior leaflet bulges into the atrium during systole
-chordae and papillary muscle -
mitral valve prolapse
-patients usually free of symptoms until condition progresses with time -
obstruction of outflow of blood from left ventricle to the aorta
-obstruction may be at the valve (semilunar), above the valve or below the valve
acquired; usually associated with rheumatic fever, degenerative calcific aortic stenosis (dystroph -
aortic stenosis
*symptoms: chest pain, loss of consciousness, heart failure and pulmonary edema -
-regurgitation is due to incomplete closure of the aortic semilunar valve
-occurs as a chronic or acute lesion depending on the disease process
-chronic lesions include lesions from rheumatic fever, syphilis, hypertension, connective tissue dis -
Aortic regurgitation, insufficiency and incompetence
*Tx: valve replacement -
-used to be a major cause of valve disease (still is in the 3rd world)
-acute phase
-chronic phase
occurs in 3% of group A Strep pharyngitis
-a hypersensitivity rxn (Type III) - deposit of antibody on antigens, also binds on valves in - Rheumatic fever
-
-Infection of the lining of the heart by bacteria(#1), fungi, rickettsiae, viruses and parasites
-Precipitating factors include contaminated needle usage, dental work or endoscopic procedures in persons with previously damaged cardiac valves
-D - Infective endocarditis
- what organism is implicated in infective endocarditis?
-
Staph. aureus
*produce friable structures that crumble off --> can embolize and colonize other sites like valve leaflets, peripheral sites - what can inflammation from bacterial endocarditis result in?
- malalignment of the valves
-
fever, hematuria, fatigue, splenomegaly, petechiae, murmur, weakness, personality changes, memory loss
Osler's node, Janeway's lesions, Roth's spots
presents acute and subacute(asymptomatic) - symptoms of infective carditis
- painful, tender, red, subcutaneous nodules in the pads of the fingers
- Osler's nodes
- flat small irregular nontender red spots on the palms and soles
- Janeway's lesions
- retinal hemorrhages that have a white or yellow center
- Roth's spots
-
severe and rapid development of symptoms including high fever, hematuria, fatigue, splenomegaly, petechiae, murmur, weakness, personality changes, memory loss
-could be fatal within days - Acute Endocarditis
-
high IV dose, prolonged antibiotic therapy strong enough to penetrate the vegetation and reach the microorganism because valves have no vasculature - med. must diffuse from blood surrounding it.
-patient given a Picc catheter and antibiotics for 6 w - Treatment of Endocarditis
-
-initiated by damage to endothelial lining on valve
-damaged areas develop a sterile fibrin deposit
-circulating organisms colonize these fibrin deposits
-peripheral lesions result from bacterial emboli from the vegetations
-emboli c - pathogenesis of endocarditis
- which organisms are implicated in bacterial endocarditis
-
Staphylococcus aureus - pathogen found on skin
– highly virulent
– seen in IV drug abusers
HACEK group - Haemophilus, Actinobacillus, Cardiobacterium, Eikenella and Kingella
– found in the oral cavity and seen following dental work -
inflammatory processes of the myocardium that results in primary injury to cardiac myocytes
causes: include infections (viral, bacteria, fungi, protozoa and helminths), immune-mediated reactions (rheumatic fever, lupus, transplant rejection) and idi - myocarditis
- Literally means heart muscle disease, but has come to mean heart disease resulting from a primary abnormality in the myocardium, 3 kinds:
-
dilated cardiomyopathy
hypertrophic cardiomyopathy
restrictive cardiomyopathy -
most common cause of sudden cardiac death in athletes; autosomal dominant disorder with defects to myosine, tropolyosin, and troponins
-results in enlarged heart w/enlarged left ventricle
-basic problem is inability to fill the hypertrophic lef -
hypertrophic cardiomyopathy
*symptoms are sudden reduce ejection fraction, harsh murmur, exertional dyspnea -
– Patent ductus arteriosus (PDA)
– Atrial septal defects
– Ventricular septal defects
– Tetralogy of Fallot
– Transposition of the great vessels - Congenital Heart Diseases-an abnormality of structure or function of the heart, circulatory system or both
-
when the the ductus arteriosus doesn't close completely at birth and there is a shunt between aorta and pulmonic arteries
-blood flows from the aorta into pulmonary circulation
Dx: 2 weeks postnatally w/harsh murmur
-results in increased v - Patent ductus arteriosus (PDA)
-
fetal opening between atria doesn't close properly
-Right ventricular hypertrophy, respiratory infections, dyspnea, fatigability are seen with larger defects - atrial septal defects
-
-Most common congenital defect
-An opening in the septum that separates the left and right ventricle doesn't close properly
-usually requires surgery - ventricular septal defects
-
-Primary cause of cyanotic heart disease
-More common in males
-Involves the combination of pulmonary stenosis, ventricular septal defect, and hypertrophy of the right ventricle
-polycythemia (compensatory) - Tetralogy of Fallot
-
right & left heart get switched, and right heart cannot maintain systemic circulation
-corrective surgery asap - Transposition of the great vessels
-
inability of the heart to eject blood delivered by the venous system; common cause of death
causes:
CAD, malformation, persistent HTN
*(but not from other causes, like cardiac tamponade) - congestive heart failure (CHF)
-
acute or insidious onset
diastolic and/or systolic dysfunction
*VENOUS return stays the same or increases. - pathophysiology of CHF
-
– Reflex increased sympathetic activity – how does this occur? baroreceptors
– Release of renin – increases volume and return to heart – mechanism for release? RAA, & stimulate brain thirst centers
– Anaerobic metabolism by affe - Systemic responses to decreased output from CHF
-
-Seen most often in patients with systemic hypertension
-Ventricle undergoes hypertrophy due to increased work load due to increased peripheral resistance
-wall enlarges --> chamber volume decreases -->ventricular compliance decreases --& -
Diastolic dysfunction with CHF
(Ventricle wall thickens) -
Seen in patients with myocardial damage due to an MI
CO declines but venous return stays the same or increases --> volume of the ventricle increases
Hypertrophy of the ventricular wall does NOT occur
*Ventricular contractili -
Systolic dysfunction with CHF
Chamber gets huge (enlarged heart) -
decrease CO --> lowers BP --> renin is released from kidney --> angiotensin --> ACE --> angiotensin II --> stimulates thirst center in brain, causes vasoconstriction, secretion of aldosterone
results: increased BP, expansion -
Renin-angiotensin-aldosterone system
(RAA)
* increases the workload on the already failing heart - Right heart failure follows left heart failure
- Right heart failure follows left heart failure
- why does an ANP draw confirm CHF?
- Atrial natriuretic peptide is release from atrial cells when there is increased stretch due to increase blood volume, as in CHF
-
-Output of the left ventricle is less than the total volume of blood received from the right side of the heart through the pulmonary circulation
-Pulmonary circuit becomes congested
-Systemic blood pressure falls
-compensatory mechanisms i - left heart failure
-
Output of right ventricle is less than the input from the system venous circuit.
-Systemic venous circuit is congested and output to the lungs decreases
-Primary cause of RHF is LHF
-Due to excessive pulmonary pressure generated by left he - Right Heart Failure